Document Detail


Possible link between right ventricular coronary sinusoids and noncompaction sinusoids in pulmonary atresia with intact ventricular septum patients that later develop left ventricular noncompaction.
MedLine Citation:
PMID:  24767937     Owner:  NLM     Status:  Publisher    
Abstract/OtherAbstract:
Patients who have pulmonary atresia with intact ventricular septum have been shown to have a number of various myocardium anomalies like ischemia, fibrosis, infarction, rupture, disarray, spongious myocardium and ventricular endocardial fibroelastosis. Multiple connections have been found between right ventricular myocardial sinusoids and small branches of intramural coronary arteries. Noncompation of ventricular myocardium has been shown to be the result of myocardial ischemia or excessive pressure preventing the reduction of embryonic sinusoids. The persistence of intertrabecular recesses that are connected to both the ventricular cavity and coronary circulation is the result of this process. In this text, we describe a PA-IVS patient who underwent patent ductus arteriosus stenting and pulmonary valve perforation to create antegrade flow and later developed left ventricular noncompaction. We posit that there is a connection between right ventricular coronary sinusoids and noncompaction sinusoids. As our patient's RV outflow tract stenosis and RV pressure increased, the coronary circulation connected to coronary sinuses became sufficient and LV function improved, which further supports our hypothesis.
Authors:
Isa Ozyilmaz; Yakup Ergul; Alper Guzeltas; Ender Odemis
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Publication Detail:
Type:  JOURNAL ARTICLE     Date:  2014-4-13
Journal Detail:
Title:  Medical hypotheses     Volume:  -     ISSN:  1532-2777     ISO Abbreviation:  Med. Hypotheses     Publication Date:  2014 Apr 
Date Detail:
Created Date:  2014-4-28     Completed Date:  -     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  7505668     Medline TA:  Med Hypotheses     Country:  -    
Other Details:
Languages:  ENG     Pagination:  -     Citation Subset:  -    
Copyright Information:
Copyright © 2014. Published by Elsevier Ltd.
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